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human and equine correlate conditions is that Henoch- Sch€
onlein purpura is not associated with an infarctive disease
involving skeletal muscles (Blanco et al. 1997; Pillebout et al. 2002). In both species, the importance of early and aggressive corticosteroid treatment cannot be emphasised enough. In previous reports of infarctive purpura haemorrhagica, such as Kaese et al. (2005), survivors were treated with high doses of corticosteroids for a prolonged period of time. This report credited the survival of these patients to largely result from high-dose corticosteroid therapy. Therefore, this mare initially received 0.2 mg/kg bwt of intravenous dexamethasone every 12 h, and was maintained on this extremely aggressive dose for 3 days. Declining serum creatine kinase concentration was used to monitor therapeutic response (Fig 3). On the day drug dose was decreased to 0.1 mg/kg bwt intravenously twice daily, CK had been stable for 3 days and clinical improvement was noted. The day the dose was decreased, CK once again increased to above 100,000 U/L. However, digital pulses were palpable and the authors elected to not increase the dose of dexamethasone again. The following day, the CK fell below 100,000 U/L, and continued to trend downwards for the remainder of hospitalisation, which was factored in to the tapering regime of the dexamethasone dosing schedule. The positive culture of Staphylococcus aureus in the
reported case was unexpected. However, there have been multiple reports of Henoch-Sch€
onlein being associated with
S. aureus in people (Hirayama et al. 1998; Yoh et al. 2000; Eftychiou et al. 2006; Temkiatvises et al. 2008; Batalille et al. 2012; Audemard-Verger et al. 2015; Maliske et al. 2015). It is speculated that in the mare of the current report, staphylococcal superantigens caused massive T-lymphocyte cell stimulation and subsequent cytokine release resulting in tissue damage, similar to what happens in human patients suffering from staphylococcal infections. Superantigens link specific variable regions of the T-cell receptor b chain (Vb) with major histocompatibility complex (MHC) class II molecules, resulting in marked expression of interleukin-1b (IL- 1b), IL-2, IL-6, IL-8 and TNF-a. Polyclonal production of IgA and IgG results in immune complex formation and a type III hypersensitivity reaction with subsequent aseptic, necrotising vasculitis (Kauffmann et al. 1980; Galen and Timoney 1985; Michel et al. 1992; Yoh et al. 2000; Eftychiou et al. 2006). Typically, S. aureus infections do not cause IMHA. In the
mare described in this report, diagnostic testing confirmed the presence of erythrocyte surface-associated IgG molecules above reference ranges. Therefore, it is hypothesised that staphylococcal antigens, potentially superantigens, triggered marked immune-mediated disease manifestation, which contributed to erythrocyte destruction in this case. Due to the rapid and intravascular nature of erythrocyte destruction marked immune system stimulation likely resulted in the presence of erythrocyte surface- associated IgG and complement-mediated intravascular haemolysis. Additionally, erythrocyte surface-associated Ig molecules contributed to extravascular cell removal by the process of Fc receptor-mediated phagocytosis by splenic macrophages (Wilkerson et al. 2000). Although the mare was clinically improved at the time of
hospital discharge, she was not normal and remained tachycardic. Ideally, repeat cardiac troponin I levels, repeat PCV and echocardiography should have been performed to
© 2017 EVJ Ltd
Source of funding None.
Authorship
All authors were involved with the management of the case described, as well as the preparation and final approval of the manuscript.
Manufacturers' addresses
1Zoetis Inc., Parsippany-Troy Hills, New Jersey, USA. 2VetOne, Boise, Idaho, USA. 3Boehringer-Ingelheim Pharmaceuticals, Inc. Ridgefield, Connecticut,
USA. 4Aurobindo Pharma USA Inc., Dayton, New Jersey, USA. 5Kentucky Performance Products LLC, Versailles, Kentucky, USA. 6Merial Inc., Duluth, Georgia, USA.
References
Audemard-Verger, A., Pillebout, E. and Guillevin, L. (2015) IgA vasculitis (Henoch- Sch€
onlein purpura) in adults: diagnostic and therapeutic aspects. Autoimmun. Rev. 14, 578-585.
Batalille, S., Daumas, A. and Tasei, A.M. (2012) Vancomycin-induced Henoch- Sch€ 106.
Blanco, R., Martınez-Taboada, V.M. and Rodrıguez-Valverde, V. (1997) Henoch–Sch€
onlein purpura: a case report. J. Med. Case Rep. 6, onlein purpura in adulthood and in childhood: two
different expressions of the same syndrome. Arthritis Rheum. 40, 859-864.
Boyle, A.G. (2016) Strangles and its complications. Equine Vet. Educ. 29, 149-157.
Duffee, L.R., Stefanovsk, D., Boston, R.C. and Boyle, A.G. (2015) Predictor variables for Streptococcus equi subspecies equi diagnosis and complications in horses: 108 cases (2005-2012). J. Am. Vet. Med. Assoc. 247, 1161-1168.
better gauge long-term prognosis; however, these additional diagnostics were declined by the owner. Because of the significant insult to her myocardium as evidenced by elevated troponin I levels and associated arrhythmia, she is at a higher risk for cardiac arrhythmias and potentially sudden cardiac death. Therefore, future riding was not recommended for this patient. In conclusion, purpura haemorrhagica and concurrent
immune-mediated disease manifestations including IMHA and myopathies typically carry a poor to grave prognosis. Most reports, in both people and horses, link the development of purpura with a previous or concurrent streptococcal infection; however, there has been increasing evidence that staphylococcal infections may also be associated with this condition. While the mare in the current report may not return to previous level of performance, early and aggressive medical management with antimicrobials and corticosteroids provided a more favourable outcome than what has previously been reported.
Authors’ declaration of interests The authors declare that there are no conflicts of interest.
Ethical animal research Not applicable for this Case Report.
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